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Helicobacter pylori and Respiratory Diseases: 2021 Update. Microorganisms 2021; 9:microorganisms9102033. [PMID: 34683354 PMCID: PMC8537719 DOI: 10.3390/microorganisms9102033] [Citation(s) in RCA: 15] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/19/2021] [Revised: 09/15/2021] [Accepted: 09/23/2021] [Indexed: 12/13/2022] Open
Abstract
Helicobacter pylori (H. pylori) is a Gram-negative bacterium involved in the development of gastritis, peptic ulcer disease, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue. Unexplained iron deficiency anemia, idiopathic thrombocytopenic purpura and vitamin B12 deficiency have also been related to H. pylori infection, whereas for other extra-gastric diseases, the debate is still open. In this review, we evaluate and discuss the potential involvement of H. pylori infection in the pathogenesis of several respiratory diseases. A MEDLINE search of all studies published in English from 1965 to 2021 was carried out. Controversial findings have been reported in patients with bronchial asthma, chronic obstructive pulmonary disease, bronchiectasis, lung cancer, tuberculosis, cystic fibrosis, and sarcoidosis. Most of the available literature is concerned with case-control studies based on seroprevalence, with a small sample size and low consideration of confounders, which represents a potential issue. So far, there is no clear evidence of a causal association between H. pylori infection and respiratory diseases, and larger studies with appropriate epidemiological design are required.
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Effect of Helicobacter pylori and Helminth Coinfection on the Immune Response to Mycobacterium tuberculosis. Curr Microbiol 2021; 78:3351-3371. [PMID: 34251513 DOI: 10.1007/s00284-021-02604-8] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/10/2021] [Accepted: 06/30/2021] [Indexed: 02/07/2023]
Abstract
Tuberculosis remains one of the main causes of morbidity and mortality worldwide despite decades of efforts to eradicate the disease. Although the immune response controls the infection in most infected individuals (90%), the ability of the bacterium to persist throughout the host's life leads to a risk of reactivation. Underlying conditions including human immunodeficiency virus (HIV) infection, organ transplantation, and immunosuppressive therapies are considered risk factors for progression to active disease. However, many individuals infected with Mycobacterium tuberculosis may develop clinical disease in the absence of underlying immunosuppression. It is also possible that unknown conditions may drive the progression to disease. The human microbiota can be an important modulator of the immune system; it can not only trigger inflammatory disorders, but also drive the response to other infectious diseases. In developing countries, chronic mucosal infections with Helicobacter pylori and helminths may be particularly important, as these infections frequently coexist throughout the host's life. However, little is known about the interactions of these pathogens with the immune system and their effects on M. tuberculosis clinical disease, if any. In this review, we discuss the potential effects of H. pylori and helminth co-infections on the immune response to M. tuberculosis. This may contribute to our understanding of host-pathogen interactions and in designing new strategies for the prevention and control of tuberculosis.
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Yuan Y, Wu Q, Cheng G, Liu X, Liu S, Luo J, Zhang A, Bian L, Chen J, Lv J, Dong X, Yang G, Zhu Y, Ma L. Recombinant human lactoferrin enhances the efficacy of triple therapy in mice infected with Helicobacter pylori. Int J Mol Med 2015; 36:363-8. [PMID: 26080893 PMCID: PMC4501646 DOI: 10.3892/ijmm.2015.2251] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/05/2015] [Accepted: 06/09/2015] [Indexed: 01/02/2023] Open
Abstract
Helicobacter pylori (H. pylori) is a life-threatening pathogen which causes chronic gastritis, gastric ulcers and even stomach cancer. Treatment normally involves bacterial eradication; however, this type of treatment only has a rate of effectiveness of <80%. Thus, it is a matter of some urgency to develop new therapeutic strategies. Lactoferrin, a member of the transferrin family of iron-binding proteins, has been proven to be effective in removing a vast range of pathogens, including H. pylori. In the present study, we examined the effectiveness of recombinant human lactoferrin (rhLf) isolated from transgenic goats as a treatment for H. pylori in vitro and in vivo. For the in vivo experiments, BALB/c mice received an intragastric administration of 0.1 ml of a suspension of H. pylori. The mice were then divided into 4 groups: group A, treated with saline; group B, treated with 1.5 g of rhLF; group C, treated with the standard triple therapy regimen; and group D, treated with the standard triple therapy regimen plus.5 g of rhLF. Following sacrifice, the stomach tissues of the mice were histologically examined for the presence of bacteria. For the in vitro experiments, the bacteria were cultured in BHI broth and RT-qPCR and western blot analysis were carried out to determine the mRNA and protein levels of virulence factors (CagA and VacA) in the cultures. Our results revealed that rhLf not only inhibited the growth of H. pylori, but also suppressed the expression of two major virulence factors. Moreover, rhLf markedly increased bacterial eradication and effectively reduced the inflammatory response when combined with the standard triple therapy regimen. These results provide evidence supporting the use of rhLF as an adjuvant to traditional therapeutic strategies in the treatment of H. pylori.
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Affiliation(s)
- Yuping Yuan
- Yunnan Institute of Digestive Disease, Department of Digestive Diseases, The First Affiliated Hospital, Kunming Medical University, Kunming, Yunnan, P.R. China
| | - Qinyi Wu
- Laboratory for Conservation and Utilization of Bio‑Resources, Yunnan University, Kunming, Yunnan, P.R. China
| | - Guoxiang Cheng
- Shanghai Jielong Bioengineering Co., Ltd., Shanghai, P.R. China
| | - Xuefang Liu
- Yunnan Institute of Digestive Disease, Department of Digestive Diseases, The First Affiliated Hospital, Kunming Medical University, Kunming, Yunnan, P.R. China
| | - Siguo Liu
- Shanghai Jielong Bioengineering Co., Ltd., Shanghai, P.R. China
| | - Juan Luo
- Yunnan Institute of Digestive Disease, Department of Digestive Diseases, The First Affiliated Hospital, Kunming Medical University, Kunming, Yunnan, P.R. China
| | - Aimin Zhang
- Shanghai Jielong Bioengineering Co., Ltd., Shanghai, P.R. China
| | - Li Bian
- Department of Pathology, The First Affiliated Hospital, Kunming Medical University, Kunming, Yunnan, P.R. China
| | - Jianquan Chen
- Shanghai Jielong Bioengineering Co., Ltd., Shanghai, P.R. China
| | - Jiajun Lv
- Yunnan Institute of Digestive Disease, Department of Digestive Diseases, The First Affiliated Hospital, Kunming Medical University, Kunming, Yunnan, P.R. China
| | - Xiangqian Dong
- Yunnan Institute of Digestive Disease, Department of Digestive Diseases, The First Affiliated Hospital, Kunming Medical University, Kunming, Yunnan, P.R. China
| | - Gang Yang
- Yunnan Institute of Digestive Disease, Department of Digestive Diseases, The First Affiliated Hospital, Kunming Medical University, Kunming, Yunnan, P.R. China
| | - Yunzhen Zhu
- Yunnan Institute of Digestive Disease, Department of Digestive Diseases, The First Affiliated Hospital, Kunming Medical University, Kunming, Yunnan, P.R. China
| | - Lanqing Ma
- Yunnan Institute of Digestive Disease, Department of Digestive Diseases, The First Affiliated Hospital, Kunming Medical University, Kunming, Yunnan, P.R. China
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Jassal MS, Nedeltchev GG, Lee JH, Choi SW, Atudorei V, Sharp ZD, Deretic V, Timmins GS, Bishai WR. 13[C]-urea breath test as a novel point-of-care biomarker for tuberculosis treatment and diagnosis. PLoS One 2010; 5:e12451. [PMID: 20805989 PMCID: PMC2929202 DOI: 10.1371/journal.pone.0012451] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/06/2010] [Accepted: 07/26/2010] [Indexed: 02/06/2023] Open
Abstract
Background Pathogen-specific metabolic pathways may be detected by breath tests based on introduction of stable isotopically-labeled substrates and detection of labeled products in exhaled breath using portable infrared spectrometers. Methodology/Principal Findings We tested whether mycobacterial urease activity could be utilized in such a breath test format as the basis of a novel biomarker and diagnostic for pulmonary TB. Sensitized New-Zealand White Rabbits underwent bronchoscopic infection with either Mycobacterium bovis or Mycobacterium tuberculosis. Rabbits were treated with 25 mg/kg of isoniazid (INH) approximately 2 months after infection when significant cavitary lung pathology was present. [13C] urea was instilled directly into the lungs of intubated rabbits at selected time points, exhaled air samples analyzed, and the kinetics of δ13CO2 formation were determined. Samples obtained prior to inoculation served as control samples for background 13CO2 conversion in the rabbit model. 13CO2, from metabolic conversion of [13C]-urea by mycobacterial urease activity, was readily detectable in the exhaled breath of infected rabbits within 15 minutes of administration. Analyses showed a rapid increase in the rate of 13CO2 formation both early in disease and prior to treatment with INH. Following INH treatment, all evaluable rabbits showed a decrease in the rate of 13CO2 formation. Conclusions/Significance Urea breath testing may provide a useful diagnostic and biomarker assay for tuberculosis and for treatment response. Future work will test specificity for M. tuberculosis using lung-targeted dry powder inhalation formulations, combined with co-administering oral urease inhibitors together with a saturating oral dose of unlabeled urea, which would prevent the δ13CO2 signal from urease-positive gastrointestinal organisms.
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Affiliation(s)
- Mandeep S Jassal
- Center for Tuberculosis Research, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
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Roussos A, Philippou N, Mantzaris GJ, Gourgoulianis KI. Respiratory diseases and Helicobacter pylori infection: is there a link? Respiration 2006; 73:708-14. [PMID: 16763382 DOI: 10.1159/000093816] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/23/2005] [Accepted: 02/28/2006] [Indexed: 12/13/2022] Open
Abstract
Recent studies suggest an epidemiological association between Helicobacter pylori infection and several extra-gastroduodenal pathologies, including cardiovascular, rheumatic, skin and liver diseases. The observed associations might be explained by a role of H. pylori infection in the pathogenesis of certain extra-digestive disorders, as a variety of inflammatory mediators are activated by H. pylori infection. The present review summarizes the current literature, including our own studies, concerning the association between respiratory diseases and H. pylori infection. A small number of epidemiological and serologic case-control studies suggest that patients with chronic obstructive pulmonary disease have an increased seroprevalence of H. pylori. A frequent coexistence of bronchiectasis and H. pylori infection has also been found. Moreover, recent studies have shown an increased prevalence of H. pylori infection in patients with pulmonary tuberculosis and in those with lung cancer. On the other hand, bronchial asthma does not seem to be related to H. pylori infection. At present, there is no definite proof of a causal relationship between H. pylori and respiratory diseases. The primary evidence rests on case-control studies, concerning relatively small numbers of patients. Future studies should be large enough for moderate-sized effects to be assessed or registered reliably. The activation of inflammatory mediators by H. pylori infection might be the pathogenetic mechanism underlying the observed associations. Therefore, the role of genetic predisposition of the infected host, the presence of strain-specific virulence factors and the serum concentration of proinflammatory markers in H. pylori-infected patients with respiratory diseases need further evaluation.
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Cianci R, Montalto M, Pandolfi F, Gasbarrini GB, Cammarota G. Third-line rescue therapy for Helicobacter pylori infection. World J Gastroenterol 2006; 12:2313-9. [PMID: 16688818 PMCID: PMC4088063 DOI: 10.3748/wjg.v12.i15.2313] [Citation(s) in RCA: 33] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
H pylori gastric infection is one of the most prevalent infectious diseases worldwide. The discovery that most upper gastrointestinal diseases are related to H pylori infection and therefore can be treated with antibiotics is an important medical advance. Currently, a first-line triple therapy based on proton pump inhibitor (PPI) or ranitidine bismuth citrate (RBC) plus two antibiotics (clarithromycin and amo-xicillin or nitroimidazole) is recommended by all consensus conferences and guidelines. Even with the correct use of this drug combination, infection can not be eradicated in up to 23% of patients. Therefore, several second line therapies have been recommended. A 7 d quadruple therapy based on PPI, bismuth, tetracycline and metronidazole is the more frequently accepted. However, with second-line therapy, bacterial eradication may fail in up to 40% of cases. When H pylori eradication is strictly indicated the choice of further treatment is controversial. Currently, a standard third-line therapy is lacking and various protocols have been proposed. Even after two consecutive failures, the most recent literature data have demonstrated that H pylori eradication can be achieved in almost all patients, even when antibiotic susceptibility is not tested. Different possibilities of empirical treatment exist and the available third-line strategies are herein reviewed.
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Gencer M, Ceylan E, Yildiz Zeyrek F, Aksoy N. Helicobacter pylori seroprevalence in patients with chronic obstructive pulmonary disease and its relation to pulmonary function tests. Respiration 2005; 74:170-5. [PMID: 16369121 DOI: 10.1159/000090158] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/30/2005] [Accepted: 08/30/2005] [Indexed: 12/16/2022] Open
Abstract
BACKGROUND Chronic obstructive pulmonary disease (COPD) is a slowly progressive condition characterized by poorly reversible airflow limitation that is associated with an abnormal inflammatory response of the lung. It has been shown that there is a seroepidemiological association of Helicobacter pylori (Hp) infection with many inflammatory conditions. OBJECTIVE In this study, we aimed to investigate seroprevalence in Hp patients with COPD and to determine whether there is an association between Hp infection and COPD. METHODS Forty-nine voluntary patients with COPD and 50 healthy control subjects of similar age and sex were included in the study. Hp-specific IgG was measured with a commercially available kit from venous blood samples. RESULTS Serum levels of Hp-specific IgG and Hp IgG seropositivity were significantly higher in the patients with COPD than in the control subjects (p < 0.001 and p = 0.006, respectively). In addition, when the patients with COPD were grouped according to Hp IgG seropositivity, forced expiratory volume in 1 s (FEV(1)) values were lower in the seropositive patients compared to seronegative patients, and Hp serum IgG levels were correlated with FEV(1) values, which indicate the severity of COPD, in the COPD group (r = -0.306, p = 0.032). CONCLUSION The results suggest that there is an association between Hp infection and COPD, and Hp IgG levels are correlated with the severity of COPD.
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Affiliation(s)
- Mehmet Gencer
- Department of Chest Diseases, Faculty of Medicine, Harran University, Sanliurfa, Turkey.
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Ahuja V, Bhatia V, Dattagupta S, Raizada A, Sharma MP. Efficacy and tolerability of rifampicin-based rescue therapy for Helicobacter pylori eradication failure in peptic ulcer disease. Dig Dis Sci 2005; 50:630-3. [PMID: 15844693 DOI: 10.1007/s10620-005-2548-2] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
In vitro activity of rifampicin has been shown against H. pylori. It has also been reported that the prevalence of H. pylori is low in patients with tuberculosis treated with rifampicin. Clinical trials are required to establish the efficacy of rifampicin as a salvage therapy for eradication of H. pylori. We aimed to evaluate the efficacy of rifampicin-based salvage therapy for eradication of H. pylori in patients with peptic ulcer disease. Twenty-eight patients with peptic ulcer disease who either had failed eradication of H. pylori or had a recurrence of H. pylori following successful eradication were included in the prospective study. The inclusion criteria included one or more failed attempts at eradication and presence of H. pylori infection as evidenced by positivity of at least two of three tests: rapid urease test (RUT), 14C urea breath test (UBT), and histology. The subjects were treated with a 10-day regimen consisting of rifampicin, 450 mg od, tetracycline, 1 g bd, and esomeprazole, 40 mg bd. Four weeks after completion of therapy, H. pylori status was assessed by RUT, 14C, UBT, and histology. Liver function tests were done before and at the end of therapy. The study subjects included 25 males and 3 females with a mean age of 33.7+/-8.92 years (range: 22-65 years). The median duration of symptoms was 42 months, with a range of 1-180 months. The median number of eradication attempts was two, with one prior attempt in 6 (21.4%), two attempts in 19 (67.9%), and three attempts in 3 (10.7%) patients. Successful H. pylori eradication as defined by concomitant negativity of RUT, UBT, and histology with special stains was achieved in 32.1% (9/28) of patients by intention-to-treat and 33.3% (9/27) of patients by per-protocol analysis. This pilot study suggests that rifampicin-based regimes have no role as salvage eradication therapy in refractory cases of H. pylori infection with peptic ulcer disease.
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Affiliation(s)
- Vineet Ahuja
- Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi, India
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Mirbagheri SA, Sohrabpour AA, Hasibi M, Moghimi B, Mohamadnejad M. 14C-urea breath test in patients undergoing anti-tuberculosis therapy. World J Gastroenterol 2005; 11:1712-4. [PMID: 15786557 PMCID: PMC4305961 DOI: 10.3748/wjg.v11.i11.1712] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: Urea breath test (UBT) is a non-invasive diagnostic test for detecting the presence of Helicobacter pylori (H pylori). In this study we evaluated the effect of anti-tuberculosis therapy on the results of 14C-UBT.
METHODS: Patients, with the diagnosis of tuberculosis (TB) who had a positive UBT at the point of starting anti-TB therapy, were included. None had a history of peptic ulcer disease or had taken antibiotics, bismuth compounds and/or PPI in the previous month. 14C-UBT was repeated at the end of the second month and the end of treatment period and one month after completion of treatment course.
RESULTS: Thirty-five patients (23 males) were enrolled. 14C-UBT was negative in all 35 patients (100%) at the end of the second month and remained negative in 30 cases (85.7%) at the end of the treatment course. One month after completion of treatment course, UBT remained negative in 13 patients (37.1%).
CONCLUSION: Our report underscores the need for caution while interpreting urea breath test results in patients undergoing anti-TB therapy. Furthermore, the combination of drugs used in this study resulted in H pylori eradication in a minority of patients.
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Affiliation(s)
- Sayed Amir Mirbagheri
- Department of Gastroenterology, Amir-Alam General Hospital, Tehran University of Medical Sciences, Tehran, Iran
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Yamamoto T, Ishii T, Kawakami T, Sase Y, Horikawa C, Aoki N, Sanaka M, Kuyama Y. Reliability of urinary tests for antibody to Helicobacter pylori in patients with pulmonary tuberculosis. World J Gastroenterol 2005; 11:412-4. [PMID: 15637756 PMCID: PMC4205350 DOI: 10.3748/wjg.v11.i3.412] [Citation(s) in RCA: 44] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: Although the quality of currently available urinary tests for detecting antibody to Helicobacter pylori (H pylori) have been proved in some populations, the accuracy has not been studied regarding patients who suffer from pulmonary tuberculosis with multi-drug treatments. The present study was conducted to evaluate the accuracy of these urinary tests for antibody to H pylori in these patients.
METHODS: Serum samples from 61 inpatients with pulmonary tuberculosis were tested using enzyme immunoassay, and urine samples were assayed by enzyme-linked immunosorbent assay method (URINELISA) and immunochromatography method (RAPIRAN). Medicines prescribed to the patients were recorded for medical charts, to evaluate the influences on the results of urinary tests.
RESULTS: The sensitivity, specificity, and consistency of URINELISA against the serum test were 93.1%, 65.6%, and 78.6% respectively, and those of RAPIRAN were 86.2%, 93.7%, and 90.1% respectively, which were almost equal to the data previously reported. Prescribed medicines had little influence on the results.
CONCLUSION: The two urinary tests for detecting H pylori antibody have a diagnostic accuracy in patients with pulmonary tuberculosis given multiple anti-tuberculosis drugs.
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Affiliation(s)
- Takatsugu Yamamoto
- Department of Internal Medicine, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8606, Japan.
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Kaneko F, Suzuki H, Hasegawa N, Kurabayshi K, Saito H, Otani S, Nakamizo H, Kawata K, Miyairi M, Ishii K, Ishii H. High prevalence rate of Helicobacter pylori resistance to clarithromycin during long-term multiple antibiotic therapy for chronic respiratory disease caused by non-tuberculous mycobacteria. Aliment Pharmacol Ther 2004; 20 Suppl 1:62-7. [PMID: 15298607 DOI: 10.1111/j.1365-2036.2004.01993.x] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
BACKGROUND Helicobacter pylori resistance to clarithromycin, probably due to the frequent use of this antibiotic for the treatment of other diseases, is the greatest obstacle against its eradication. AIM To clarify the prevalence of clarithromycin-resistant H. pylori in patients with non-tuberculous mycobacterial lung disease receiving multiple antibiotic treatment, including clarithromycin. METHODS We enrolled 88 patients with non-tuberculous mycobacterial lung disease; 29 underwent upper gastrointestinal endoscopy for the diagnosis of H. pylori infection prior to treatment, and 60 underwent it during treatment. The diagnosis of H. pylori infection was confirmed by histological examination, urease test and microaerobic bacterial culture. The minimum inhibitory concentration of clarithromycin was determined and the DNA was analysed for each of the isolated H. pylori strains. RESULTS Patients during the treatment had a high prevalence rate of clarithromycin-resistant H. pylori (100%). Analysis of DNA of the clarithromycin-resistant H. pylori isolates revealed point mutations at A2142G or A2143G. Moreover, a linear correlation was found between the total cumulative dose of clarithromycin and the minimum inhibitory concentration. CONCLUSION All patients with non-tuberculous mycobacterial lung disease being treated long-term with multiple antibiotics, including clarithromycin, harboured clarithromycin-resistant H. pylori in the stomach. Therefore, eradication of H. pylori before commencement of long-term therapy including clarithromycin should be recommended.
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Affiliation(s)
- F Kaneko
- National Minami-Yokohama Hospital, Tokyo, Japan
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Abstract
In the past few years, a variety of extradigestive disorders, including cardiovascular, skin, rheumatic and liver diseases, have been associated with Helicobacter pylori (H. pylori) infection. The activation of inflammatory mediators by H. pylori seems to be the pathogenetic mechanism underlying the observed associations. The present review summarizes the current literature, including our own studies, concerning the association between H. pylori infection and respiratory diseases.
A small number of epidemiological and serologic, case-control studies suggest that H. pylori infection may be associated with the development of chronic bronchitis. A frequent coexistence of pulmonary tuberculosis and H. pylori infection has also been found. Moreover, recent studies have shown an increased H. pylori seroprevalence in patients with bronchiectasis and in those with lung cancer. On the other hand, bronchial asthma seems not to be related with H. pylori infection.
All associations between H. pylori infection and respiratory diseases are primarily based on case-control studies, concerning relatively small numbers of patients. Moreover, there is a lack of studies focused on the pathogenetic link between respiratory diseases and H. pylori infection. Therefore, we believe that larger studies should be undertaken to confirm the observed results and to clarify the underlying pathogenetic mechanisms.
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Affiliation(s)
- Anastasios Roussos
- 9th Department of Pulmonary Medicine, SOTIRIA Chest Diseases Hospital, Athens, Greece.
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